D-galactose (D-gal), a physiological nutrient derived from lactose in milk, is metabolized in animals by D-galactokinase and galactose-1-phosphate uridyltransferase. Research has shown that D-gal treated animals showed some hallmarks of aging, such as a shortened life span, cognitive dysfunction, presbycusis, increased oxidative stress, decreased antioxidant enzyme activity, diminished immune responses, increased advanced glycation endproducts (AGEs), accumulation of mitochondrial DNA (mtDNA) mutations, and mitochondrial dysfunction.
Mitochondria are not only the major sites of intracellular reactive oxygen species (ROS) production, but also targets of ROS. This ROS-induced oxidative damage contributes to mitochondrial dysfunction, which in turn produces more ROS. This vicious cycle of ROS production and oxidative damage in the mitochondria suggests that mitochondrial dysfunction plays an important role in the aging process.